First, a disclaimer: I am not an expert on the details of altitude sickness. I am a chemist, not an MD or a physiologist, or even a mountaineer. I understand some of the chemistry of altitude sickness, and in writing these pieces I am trying to stay out of places where my knowledge is limited. If you are interested in the medical, symptomatic or preventive aspects of altitude sickness, please look elsewhere. My coverage here is limited to some of the chemical features of altitude sickness that can be explained in common language.
Acute Mountain Sickness is an “entry level” form of altitude sickness, the least aggressive of the three forms. Nevertheless, AMS is not a condition that should underestimated. It can be dangerous in its own right and can be an indicator of more threatening stages of altitude sickness.
Climbing to altitude without proper acclimatization can result in the accumulation of water in the lungs, a form of altitude sickness known as High Altitude Pulmonary Edema (HAPE). Water collects in the lungs by seeping across a thin membrane that separates the air-filled alveoli from the blood-filled capillaries. That lower atmospheric pressure described in Part 2 goes all the way down to the alveoli. Fewer molecules per lungful of air translates to lower pressure in the alveoli. It’s the pressure differential across the capillary-alveoli membrane that matters. Lower pressure in the alveoli “pulls” water across the membrane from the higher-pressure capillaries. There’s a lot more to this, of course. For example, hypoxia also triggers a constriction of the capillaries, presumably to increase the rate of blood flow and hasten the collection of oxygen. This higher pressure in the capillaries “pushes” water molecules from the higher-pressure capillaries to the lower-pressure alveoli. These effects, and others, lead to the same outcome: Gradually, the alveoli fill with water. High Altitude Pulmonary Edema is the leading cause of death from altitude sickness. Onset usually doesn’t occur below 8,000’, but cases down to 5,000’ are known. Fortunately, the symptoms of HAPE are obvious and graduated. The clearest indicator is a rasping cough on top of AMS symptoms. Again, this is not meant to be a complete coverage of HAPE. Readers are urged to consult other sources.
The third form of altitude sickness is High Altitude Cerebral Edema (HACE). I don't have much to say here. HACE is similar to HAPE in that the condition is about the accumulation of water. In this case, water collects in the brain rather than the lungs. HACE is an uncommon form of altitude sickness. The condition is observed is less than 1% of climbers who ascend to 13,000’. While rare, however, HACE is very dangerous. I am not familiar with the mechanism of HACE, but it appears to involve similar capillary-tissue pressure differentials characteristic of HAPE. Water is forced from the capillaries into the cranial tissue.
For further information, I recommend "Medicine for Mountaineering" by James Wilkerson, Mountaineers Books. My older edition has an excellent chapter on the effects of altitude. I did learn one very interesting thing here about very high-altitude mountaineering. In the death zone, climbers cannot acquire enough oxygen to survive. In fact, they barely collect enough oxygen to sustain their breathing. Breathing takes work, of course, and way high up there, so much breathing has to be done that the amount of work involved in that breathing is barely covered by the oxygen taken in by all that breathing. There isn't enough O2 left over to energize anything else. Life is unsustainable in the death zone because (at least in part) virtually all the oxygen taken in by breathing is used up to fuel even more breathing. It's a death spiral
Next up: Acclimatization